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Dendritic cells regulate the innate-adaptive balance in lymph nodes for optimal host defense

ABSTRACT: Dendritic cells regulate the innate-adaptive balance in lymph nodes for optimal host defense

PROVIDER: PRJNA1217051 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32174149_1.fastq.gz	Fastqsanger.gz
	SRR32174149_2.fastq.gz	Fastqsanger.gz
	SRR32174150_1.fastq.gz	Fastqsanger.gz
	SRR32174150_2.fastq.gz	Fastqsanger.gz
	SRR32174151_1.fastq.gz	Fastqsanger.gz

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Dendritic cells regulate the innate-adaptive balance in lymph nodes for optimal host defense

Project description:Lymph nodes (LNs) enable innate defense to limit pathogen dissemination while also driving adaptive immunity. Yet, certain innate responses can restrict adaptive processes, suggesting that these must be tightly regulated. Here, we report that after infection or immunization, LN architecture is rapidly altered, with large-scale, polarized recruitment of neutrophils and monocytes from inflamed blood vessels, and intranodal repositioning of NK cells. Mechanistically, dendritic cells (DCs) promote this process through expression of inflammatory chemokines and integrin ligands. While necessary for efficient pathogen containment, DC-driven innate cell responses paradoxically limit early adaptive immunity, with infiltrating neutrophils displacing lymphocytes and reducing the LN area available for T cell priming. Upon threat secession however, DCs and DC-recruited monocytes phagocytose the neutrophils, restoring tissue architecture and generating polarized domains for downstream adaptive immune cell activation. Thus, DCs orchestrate innate cell organization during inflammation, serving as rheostats of innate versus adaptive functions of the LN.

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scRNAseq of stromal cells isolated from mesenteric lymph nodes (MLN), peripheral lymph nodes (PLN) and mandibular lymph nodes (mandLN)

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Transcription Profiles of Regulatory T Cells in Follicular Lymphoma Lymph Nodes, Normal Lymph Nodes and Reactive Lymph Nodes

Project description:We have previously shown that Tregs infiltrating follicular lymphoma lymph nodes (FLN) are quantitatively and qualitatively different than those infiltrating normal and reactive nodes (NLN, RLN, respectively). To gain insight into how such Treg populations differ, we performed RNA sequence (RNAseq) analyses on flow sorted Tregs from all three sources. We identify several molecules that could contribute to the observed increased suppressive capacity of FLN tregs, including upregulation of CTLA-4, IL-10, and GITR, all confirmed by protein expression. In addition, we identify, and confirm functionally, a novel mechanism by which Tregs target to and accumulate within a human tumor microenvironment, through the down regulation of S1PR1, SELL (L-selectin) and CCR7, potentially resulting in greater lymph node retention. In addition we identify and confirm functionally the upregulation of CXCR5, CXCL13 and IL-16 demonstrating the unique ability of the follicular derived Tregs to localize and accumulate within not only the malignant lymph node, but also localize and accumulate within the malignant B cell follicle itself. Such findings offer significant new insights into how FLN Tregs may contribute to the biology of follicular lymphoma and identify several novel therapeutic targets.

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Project description:To determine the influence of primary tumors on pre-metastatic lymph nodes, we have employed whole genome microarray expression profiling as a discovery platform to identify gene signatures of B cells from tumor-draining lymph nodes, compared with normal lymph nodes. We subcutaneously inoculated C57BL/6 mice with the 4T1 mammary carcinoma. Two weeks later, tumor-draining lymph nodes were dissociated and B cells (CD19+) were sorted. Lymph nodes B cells from normal mice without tumor bearing were set as controls.

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